Nicotine stimulates adrenergic terminals and inhibits contractions of mouse uterine horns

Abstract

1. Nicotine (1-100 microM) stimulated both basal and electrically evoked release of 3H-norepinephrine and also caused a transient inhibition of contractions in an in vitro preparation of mouse uterine horns. 2. The inhibitory effect of nicotine on electrically evoked contractions was potentiated by aminophylline (89 micrograms/ml), and overcome by both propranolol (1 microM) and by omitting magnesium from the physiological solution. Acetylcholine (10 microM), in the presence of atropine (10 microM) was able to reproduce the inhibitory effect of nicotine. 3. These pharmacological findings suggest that the inhibitory action of nicotine on electrically evoked contractions in mouse uterus could be indirect, i.e. mediated through the action of this compound on presynaptic nicotine receptors located on adrenergic terminals.